Firstly, there is a nice time series chart courtesy of the Saw Swee Hock School of Public Health team, showing a rise in blood isolates of GBS (signifying severe infection) from March 2015, whereas the number of GBS isolates cultured from all other body sites did not increase over the same time period.

A = GBS from blood. B = GBS from all other human sites. Data from most public sector hospital microbiology laboratories in Singapore. Snapshot from the CID publication.

The corresponding clinical comparison between local adults infected with ST283 GBS (n=146) vs. non-ST283 GBS (non=262) in their blood showed that those infected with the outbreak strain of GBS:

Were younger

Were more likely to have consumed raw fish just prior to the infection

Had fewer co-morbid conditions like diabetes mellitus or cancer

Were more likely to have brain involvement (19.9% vs. 0%) and joint involvement (30.1% vs. 5.0%) but less likely to have skin (18.5% vs. 42.0%) or urinary tract (3.4% vs 11.8%) involvement.

But were not more likely to die as a result of the ST283 GBS infection.

We were also able to get ST283 GBS isolates from Hong Kong courtesy of Prof Margaret Ip, who studied the original cases in Hong Kong in 2006, and also from Bangkok courtesy of Prof Anucha Apisarnthanarak, who described a similar outbreak in Thailand in 2015.

Excellent work by Dr Swaine Chen (GIS) and Prof Matthew Holden (St Andrews University, Scotland) analysing the entire genomes of the Singapore, Hong Kong and Thailand isolates showed that they were strikingly similar, and in fact, the Singaporean GBS isolates from humans (and the rare fish ST283 GBS we were able to obtain and sequence from Singapore General Hospital and the Environmental Health Institute) were clustered so closely together and with so few single nucleotide polymorphisms (SNPs) that the genomic data and results virtually suggested a point source outbreak in the Singapore context. The human and fish genomic results also virtually resolves the link between raw fish consumption and human disease.

Although the outbreak occurred in 2015, ST283 GBS has already been causing human infections in Singapore since at least 2012, with increasing numbers each year until the fateful events of 2015.

What do we still not know after doing this work?

The exact source of the outbreak remains unknown. At which point were the fish infected (at the farms themselves, or somewhere during the logistics chain down to Singapore)?

Why is the clinical presentation different between this “special” clone of GBS as compared to other GBS infections?

We know lots of people (used to) consume raw yusheng at porridge stalls – far more than the number actually infected with ST283 GBS. Why did the rest not get the infection? Was it a matter of lower infectious “dose” or some kind of immune defect? This is also not clear at present.